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首页> 外文期刊>BMC Neuroscience >Lithium facilitates apoptotic signaling induced by activation of the Fas death domain-containing receptor
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Lithium facilitates apoptotic signaling induced by activation of the Fas death domain-containing receptor

机译：锂促进由激活的含Fas死亡域的受体激活而诱导的凋亡信号转导

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Background Lithium, a mood stabilizer widely used to treat bipolar disorder, also is a neuroprotectant, providing neurons protection from apoptosis induced by a broad spectrum of toxic conditions. A portion of this neuroprotection is due to lithium's inhibition of glycogen synthase kinase-3. The present investigation examined if the neuroprotection provided by lithium included apoptosis induced by stimulation of the death domain-containing receptor Fas. Results Instead of providing protection, treatment with 20 mM lithium significantly increased apoptotic signaling induced by activation of Fas, and this occurred in both Jurkat cells and differentiated immortalized hippocampal neurons. Other inhibitors of glycogen synthase kinase-3, including 20 μM indirubin-3'-monoxime, 5 μM kenpaullone, and 5 μM rottlerin, also facilitated Fas-induced apoptotic signaling, indicating that the facilitation of apoptosis by lithium was due to inhibition of glycogen synthase kinase-3. Conclusions These results demonstrate that lithium is not always a neuroprotectant, and it has the opposite effect of facilitating apoptosis mediated by stimulation of death domain-containing receptors.
机译：背景技术锂，一种广泛用于治疗躁郁症的情绪稳定剂，也是一种神经保护剂，可为神经元提供保护，使其免受各种毒性条件引起的细胞凋亡。这种神经保护作用的一部分归因于锂对糖原合酶激酶-3的抑制作用。本研究检查了锂提供的神经保护作用是否包括通过刺激包含死亡域的受体Fas诱导的凋亡。结果用20 mM锂而不是提供保护，显着增加了Fas激活诱导的凋亡信号转导，这发生在Jurkat细胞和已分化的永生海马神经元中。糖原合酶激酶3的其他抑制剂，包括20μM靛玉红3'-一肟，5μM肯帕龙和5μMrottlerin，也促进Fas诱导的凋亡信号传导，表明锂促凋亡是由于糖原的抑制引起的合酶激酶3。结论这些结果表明，锂并不总是一种神经保护剂，它具有促进通过刺激包含死亡域的受体介导的细胞凋亡的相反作用。

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